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In vivo Metabolic Defects in Non-lnsulin-Dependent Diabetes mellitus

In vivo Metabolic Defects in Non-lnsulin-Dependent Diabetes mellitus In patients with non-insulin-dependent diabetes mellitus (NIDDM) alterations in insulin secretion and insulin action coexist, and create and sustain hyperglycaemia, which results from an imbalance between glucose production and glucose utilization. The target organs for insulin action are the liver (restriction of glucose production), the muscle (acceleration of glucose disposal) and the adipose tissue (inhibition of free fatty acid mobilization). In NIDDM, the liver produces an inordinate amount of glucose, secondary to an acceleration of gluconeogenesis, and is insensitive to the inhibitory action of insulin on glucose production. In NIDDM, skeletal muscle takes up less glucose in response to hyperinsulinaemia. Adipose tissue mobilizes a larger amount of free fatty acid, thereby possibly enhancing glucose production in the liver (Randle’s cycle of metabolic competition between free fatty acids and glucose). Thus, the in vivo assessment of insulin action in NIDDM reveals a web of possibly interrelated metabolic defects, which in association with impaired insulin secretion cause a permanent, profound disruption of glucose homoeostasis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hormone Research in Paediatrics Karger

In vivo Metabolic Defects in Non-lnsulin-Dependent Diabetes mellitus

Bonadonna, R.C.
Hormone Research in Paediatrics , Volume 39 (Suppl 3): 5 – Jan 1, 1993
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Publisher
Karger
Copyright
© 1993 S. Karger AG, Basel
ISSN
1663-2818
eISSN
1663-2826
DOI
10.1159/000182794
Publisher site
See Article on Publisher Site

Abstract

In patients with non-insulin-dependent diabetes mellitus (NIDDM) alterations in insulin secretion and insulin action coexist, and create and sustain hyperglycaemia, which results from an imbalance between glucose production and glucose utilization. The target organs for insulin action are the liver (restriction of glucose production), the muscle (acceleration of glucose disposal) and the adipose tissue (inhibition of free fatty acid mobilization). In NIDDM, the liver produces an inordinate amount of glucose, secondary to an acceleration of gluconeogenesis, and is insensitive to the inhibitory action of insulin on glucose production. In NIDDM, skeletal muscle takes up less glucose in response to hyperinsulinaemia. Adipose tissue mobilizes a larger amount of free fatty acid, thereby possibly enhancing glucose production in the liver (Randle’s cycle of metabolic competition between free fatty acids and glucose). Thus, the in vivo assessment of insulin action in NIDDM reveals a web of possibly interrelated metabolic defects, which in association with impaired insulin secretion cause a permanent, profound disruption of glucose homoeostasis.

Journal

Hormone Research in Paediatrics – Karger

Published: Jan 1, 1993

Keywords: Non-insulin-dependent diabetes mellitus; Glucose metabolism; Gluconeogenesis; Glycogen synthesis

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